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Interaction between DNA Polymerase b and BRCA1
https://repo.qst.go.jp/records/46931
https://repo.qst.go.jp/records/469313857853d-4dfe-4dd8-abad-3b974e89b7d2
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2014-11-13 | |||||
| タイトル | ||||||
| タイトル | Interaction between DNA Polymerase b and BRCA1 | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Masaoka, Aya
× Masaoka, Aya× Wilson, Samuel× et.al× 正岡 綾 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | The breast cancer 1 (BRCA1) protein is a tumor suppressor playing roles in DNA repair and cell cycle regulation. Studies of DNA repair functions of BRCA1 have focused on double-strand break (DSB) repair pathways and have recently included base excision repair (BER). However, the function of BRCA1 in BER is not well defined. Here, we examined a BRCA1 role in BER, first in relation to alkylating agent (MMS) treatment of cells and the BER enzyme DNA polymerase b (pol b). MMS treatment of BRCA1 negative human ovarian and chicken DT40 cells revealed hypersensitivity, and the combined gene deletion of BRCA1 and pol b in DT40 cells was consistent with these factors acting in the same repair pathway, possibly BER. Using cell extracts and purified proteins, BRCA1 and pol b were found to interact in immunoprecipitation assays, yet in vivo and in vitro assays for a BER role of BRCA1 were negative. An alternate approach with the human cells of immunofluorescence imaging and laser-induced DNA damage revealed negligible BRCA1 recruitment during the first 60 s after irradiation, the period typical of recruitment of pol b and other BER factors. Instead, 15 min after irradiation, BRCA1 recruitment was strong and there was c- H2AX co-localization, consistent with DSBs and repair. The rapid recruitment of pol b was similar in BRCA1 positive and negative cells. However, a fraction of pol b initially recruited remained associated with damage sites much longer in BRCA1 positive than negative cells. Interestingly, pol b expression was required for BRCA1 recruitment, suggesting a partnership between these repair factors in DSB repair. | |||||
| 書誌情報 |
PLoS ONE (Online only:URL:http://www.plosone.org) 巻 8, 号 6, p. e66801, 発行日 2013-06 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1932-6203 | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1371/journal.pone.0066801 | |||||
